The current study is based on the original observation that chronic lead exposure of neonatal rats produces adults especially sensitive to the arrhythmogenic effects of norepinephrine. Experminents have previously shown that 1) both direct and indirect (reflex) components of the cardiac norepinephrine response are enhanced; 2) exposure during the first ten days of life is critical for expression of the response; 3) maintenance of elevated tissue lead levels until adulthood is not necessary; 4) concentrations of the adrenergic neurotransmitter, norepinephrine, in tissues, including heart, are altered by early lead exposure; and 5) lead exposure enhances the cardiac response to the cholinergic agonist, methacholine. Future work will concentrate on the effects of early lead exposure on development of cardiac autonomic systems. Adrenergic development will be monitored by examining the norepinephrine concentration and uptake capacity of the heart during lead exposure. Both properties increase during the first ten days of normal development. The cholinergic nervous system will be monitored as the development of cholinergic receptor number and sensitivity, using ligand binding techniques. In addition, specificity of the lead effect will be tested using drugs other than norepinephrine to produce cardiac arrhythmias.